Mice of the C57BL/6ByJ (B6) strain have higher consumption of sucrose, and stronger peripheral neural responses to it, than do mice of the 129P3/J (129) strain. To identify quantitative trait loci (QTLs) responsible for this strain difference and to evaluate the contribution of peripheral taste responsiveness to individual differences in sucrose intake, we produced an intercross (F₂) of 627 mice, measured their sucrose consumption in two-bottle choice tests, recorded the electrophysiological activity of the chorda tympani nerve elicited by sucrose in a subset of F₂ mice, and genotyped the mice with DNA markers distributed in every mouse chromosome. We confirmed a sucrose consumption QTL (Scon2, or Sac) on mouse chromosome (Chr) 4, harboring the Tas1r3 gene, which encodes the sweet taste receptor subunit TAS1R3 and affects both behavioral and neural responses to sucrose. For sucrose consumption, we also detected five new main-effect QTLs, Scon6 (Chr2), Scon7 (Chr5), Scon8 (Chr8), Scon3 (Chr9), and Scon9 (Chr15), and an epistatically interacting QTL pair Scon4 (Chr1) and Scon3 (Chr9). No additional QTLs for the taste nerve responses to sucrose were detected besides Scon2 (Tas1r3) on Chr4. Identification of the causal genes and variants for these sucrose consumption QTLs may point to novel mechanisms beyond peripheral taste sensitivity that could be harnessed to control obesity and diabetes.

与 129P3/J (129) 品系的小鼠相比，C57BL/6ByJ (B6) 品系的小鼠对蔗糖的消耗量更高，外周神经反应更强。为了确定导致这种菌株差异的数量性状基因座 (QTL) 并评估外周味觉反应对蔗糖摄入个体差异的贡献，我们对 627 只小鼠进行了杂交 (F ₂ )，测量了它们在两瓶选择中的蔗糖消耗量测试中，记录了 F ₂小鼠亚群中蔗糖引起的鼓索神经的电生理活动，并用分布在每个小鼠染色体中的 DNA 标记对小鼠进行基因分型。我们证实了一个小号ucrose CON sumption QTL（Scon2，或 Sac ) 在小鼠染色体 (Chr) 4 上，含有Tas1r3基因，该基因编码甜味受体亚基 TAS1R3 并影响对蔗糖的行为和神经反应。对于蔗糖消耗，我们还检测到五个新的主效应 QTL，Scon6 (Chr2) 、Scon7 (Chr5) 、Scon8 (Chr8) 、Scon3 (Chr9) 和Scon9 (Chr15)，以及一个上位相互作用的 QTL 对Scon4 (Chr1)和 Scon3 (Chr9)。除了Scon2 ( Tas1r3) 在 Chr4 上。对这些蔗糖消耗 QTL 的因果基因和变异的鉴定可能会指出可用于控制肥胖和糖尿病的外周味觉敏感性之外的新机制。